Polley M J, Müller-Eberhard H J, Feldman J D
J Exp Med. 1971 Jan 1;133(1):53-62. doi: 10.1084/jem.133.1.53.
A direct quantitative relationship has been demonstrated between the number of cell bound C4,2 complexes or C5 molecules and the number of ultrastructural lesions visualized on the cell membrane subsequent to immune hemolysis. When bound C4,2 complexes exceeded bound C5 molecules, the number of ultrastructural lesions seen corresponded to the number of C5 molecules. However, in the reverse situation, with bound C5 molecules in excess of bound C4,2 complexes, the latter determined the number of lesions. During the complement-reaction sequence, the lesions first became visible in the nonlytic intermediate complex EAC1,4,2,3,5 and their number was unaffected when lysis was induced by C6-C9. Since the lesions were also demonstrable on the intermediate complex EC5,6,7, it is concluded that the protein C5 is responsible for their production. Once formed, the physical presence of the C5 molecule is no longer required for the manifestation of the lesions as indicated by persistence of lesions after removal of C5 protein by trypsin. The C5-dependent ultra-structural phenomenon has therefore been interpreted to represent a true structural change of the membrane which, however, is not accompanied by a permeability defect.
已证明细胞结合的C4,2复合物或C5分子的数量与免疫溶血后在细胞膜上可见的超微结构损伤数量之间存在直接定量关系。当结合的C4,2复合物超过结合的C5分子时，所见超微结构损伤的数量与C5分子的数量相对应。然而，在相反的情况下，即结合的C5分子超过结合的C4,2复合物时，则由后者决定损伤的数量。在补体反应序列中，损伤首先在非溶细胞性中间复合物EAC1,4,2,3,5中可见，并且当由C6 - C9诱导裂解时，其数量不受影响。由于在中间复合物EC5,6,7上也可证明存在损伤，因此得出结论，蛋白质C5负责损伤的产生。一旦形成，如用胰蛋白酶去除C5蛋白后损伤仍持续存在所示，损伤的表现不再需要C5分子的实际存在。因此，这种C5依赖性超微结构现象被解释为代表膜的真正结构变化，然而，这种变化并不伴有通透性缺陷。
